ajmaline and lorcainide

A number of conventional and newer antiarrhythmic agents are available for the treatment and prophylaxis of ventricular tachycardia and sudden death. Using a multifaceted approach of programmed electrical stimulation studies, drug level determinations, exercise tolerance testing, and 24-hour ambulatory electrocardiographic monitoring, the physician can identify those patients who require therapy and then predict the likelihood of efficacy with each antiarrhythmic agent. This approach affords evaluation of both aspects of the sudden death equation-ectopy frequency (triggering mechanism) and vulnerability to development of sustained ventricular tachycardia (substrate). After institution of therapy, careful follow-up is necessary to document sustained drug efficacy and detect side effects. Serious adverse reactions necessitate a change in antiarrhythmic therapy, as opposed to lowering drug dosage to an ineffective level. The unacceptably high incidence of sudden death due to electrical instability can be reversed only by a rigorous and dedicated long-term approach to the management of serious ventricular arrhythmias.

Topics: Adrenergic beta-Antagonists; Ajmaline; Amiodarone; Anilides; Anti-Arrhythmia Agents; Aprindine; Arrhythmias, Cardiac; Benzeneacetamides; Bepridil; Bethanidine; Bretylium Tosylate; Disopyramide; Drug Administration Schedule; Encainide; Flecainide; Heart Conduction System; Humans; Imidazoles; Lidocaine; Mexiletine; Moricizine; Myocardial Contraction; Phenothiazines; Phenytoin; Piperidines; Procainamide; Propafenone; Propiophenones; Pyrrolidines; Quinidine; Tocainide; Verapamil

Topics: Action Potentials; Ajmaline; Amiodarone; Anilides; Animals; Anti-Arrhythmia Agents; Aprindine; Arrhythmias, Cardiac; Benzeneacetamides; Bretylium Tosylate; Disopyramide; Encainide; Hemodynamics; Humans; Kinetics; Moricizine; Morpholines; Phenothiazines; Piperidines; Verapamil

Clinical safety and hemodynamic repercussions were studied after administration of six class I antiarrhythmics (xylocaine, ajmaline, mexiletine, lorcainide, indecainide and tocainide) to patients presenting acute myocardial infarction without complications. The hemodynamic parameters monitored generally followed the same trends. A significant decrease of more than 10 per cent of the initial value was seen in systolic blood flow after injection of lorcainide, indecainide and tocainide. Peripheral vascular resistance increased moderately. Pulmonary capillary pressure increased by more than 40 per cent of the starting value after administration of mexiletine, indecainide and tocainide (significant increase in case of mexiletine). These changes in patients presenting infarction without complications are not of clinical importance. There were, however, two very severe cases of hemodynamic reaction after administration of mexiletine. Other signs of intolerance were seen, but they were of minor importance and administration of the drugs was not interrupted. Xylocaine and ajmaline produced the smallest depression of left ventricular functional activity in these patients.

Topics: Ajmaline; Anti-Arrhythmia Agents; Benzeneacetamides; Fluorenes; Hemodynamics; Lidocaine; Mexiletine; Myocardial Infarction; Piperidines; Tocainide

Cardiac arrhythmia causing sudden cardiac death is a serious worldwide public health problem. Antiarrhythmic agents have been available for therapy, but the conventional agents cause a high degree of intolerable side effects. The recent development of many new experimental antiarrhythmic agents has increased our capacity to effectively treat cardiac arrhythmias. Using a multifaceted approach of programmed electrical stimulation studies, drug level determinations, exercise testing and 24-hour ambulatory Holter monitoring, it can reasonably be decided which patient needs therapy and if therapy is going to be effective. Both aspects of the sudden death equation, ectopy frequency (triggering mechanism) and the ability to propagate sustained ventricular tachycardia (substrate), may be examined. Careful follow-up is needed to determine continued drug efficacy and the presence of side effects that may compromise patient compliance with therapy. If side effects intervene that may cause continued therapy to be intolerable, changing the antiarrhythmic agent, as opposed to decreasing the dosage to an ineffective range, may be appropriate. A comprehensive approach to arrhythmia management may begin to reduce the high incidence of sudden death due to fatal arrhythmias.

Topics: Adrenergic beta-Antagonists; Ajmaline; Amiodarone; Anilides; Anti-Arrhythmia Agents; Aprindine; Benzeneacetamides; Bepridil; Bethanidine; Bretylium Tosylate; Death, Sudden; Disopyramide; Encainide; Flecainide; Humans; Lidocaine; Mexiletine; Moricizine; Phenothiazines; Piperidines; Procainamide; Propafenone; Propiophenones; Pyrrolidines; Quinidine; Tachycardia; Tocainide; Verapamil

The widespread use of antiarrhythmic agents to control severe life-threatening arrhythmias evidenced the possibility of a worsening of arrhythmias induced by the same drugs. We performed a retrospective analysis studying the worsening phenomenon in patients who underwent pharmacological invasive and non invasive antiarrhythmic tests to choose the drug to be administered in the chronic treatment. Particularly we reviewed: 101 acute pharmacologic non invasive tests for "stable" ventricular ectopic beats using computerized automatic continuous recording system which allows quantitative and qualitative evaluation of arrhythmias. The drugs tested were: Propafenone (25 patients), Disopiramide (25 patients), Tocainide (11 patients), Lorcainide (8 patients), Lorajmine (13 patients), Nadolol (9 patients). In accordance with Vallebit et al., we considered arrhythmias worsening criteria: the onset of non sustained or sustained ventricular tachycardia; an increase of four fold the number of ventricular ectopic beats and/or ten fold the repetitive forms. A worsening of arrhythmias was observed in 4/101 (3.9% patients); 1/9 treated with Nadolol, 1/25 with Propafenone, 1/35 with Disopiramide, 1/13 with Lorajmine. For one young patient the worsening phenomenon could be considered a toxic picture, because of the very high drug plasmatic levels (Lorajmine) observed for the whole duration of the sustained VT induced from the drug. For the remaining 3 patients the response resambles a paradox effect. 34 pharmacologic invasive tests in 30 patients with common recurrent ventricular tachycardia, during electrophysiologic endocavitary study. The drugs tested were: Propafenone (12 patients), Amiodarone (11 patients), Ajmaline (4 patients), Tocainide (3 patients), Lorcainide (2 patients), Lorajmine (1 patient), Disopiramide (1 patient).(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adolescent; Adult; Aged; Ajmaline; Amiodarone; Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Benzeneacetamides; Child; Disopyramide; Female; Follow-Up Studies; Humans; Lidocaine; Male; Middle Aged; Nadolol; Piperidines; Propafenone; Propanolamines; Propiophenones; Tocainide

Topics: Adult; Aged; Ajmaline; Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Benzeneacetamides; Electrocardiography; Female; Humans; Male; Middle Aged; Piperidines; Syncope; Time Factors